MR imaging findings in hepatic encephalopathy

Abstract

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.

Fig 1.

Transverse T1-weighted MR images of the brain in a patient with chronic liver failure and parkinsonism. Observe the bilateral and symmetric high T1 signal-intensity change involving the globus pallidus and the anterior midbrain.

Fig 2.

¹H-MR-spectroscopy water-suppressed proton spectra of an 8-mL voxel located in the parietal region including predominantly normal-appearing white matter in a patient with cirrhosis before (left) and after (right) liver transplantation, recorded with a stimulated echo acquisition mode pulse sequence (TR/TE, 1600/20 ms; acquisitions, 256). The main resonances correspond to N-acetylaspartate (NAA, 2.0 ppm), glutamine/glutamate (Glx, 2.1–2.5 ppm), creatine/phosphocreatine (Cr, 3.02 ppm), choline-containing compounds (Cho, 3.2 ppm), and myo-inositol (Ins, 3.55 ppm). The initial spectrum shows an increase in the glutamate/glutamine region and a decrease in the myo-inositol and choline resonances. These abnormalities normalized after liver transplantation. Normal NAA indices are seen in both examinations.

Fig 3.

A, Transverse T2-weighted fast FLAIR images obtained in a patient with liver cirrhosis during an episode of hepatic encephalopathy. Observe the symmetric areas of increased signal intensity along the corticospinal tract in both cerebral hemispheres. B, This signal-intensity abnormality almost completely reverses on a follow-up study obtained few months later, when the patient showed no signs of overt hepatic encephalopathy.

Fig 4.

A, Baseline MR imaging study (transverse fast FLAIR T2-weighted image) of a 56-year-old patient with hepatitis C cirrhosis without overt hepatic encephalopathy. Multiple focal WMLs in both cerebral hemispheres are attributed to small-vessel disease. B, A new scan obtained 2 years later during an episode of hepatic encephalopathy shows marked increase in the size of these focal WMLs. C, A new follow-up scan after complete resolution of neurologic symptoms shows a decrease in the size of the WMLs. This last scan was almost identical to the first study. A lacunar infarct is seen in the deep right frontal white matter.