Article Figures & Data
Figures
- 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.
Tables
HE Liver Disease Extrahepatic Portal-Systemic Shunting Neurologic Manifestations Specific Features Acute episode In cirrhosis Cirrhosis Variable Acute confusional state to coma Usually precipitated In acute liver failure Acute liver failure Absent Acute confusional state to coma Frequently complicated by brain edema and intracranial hypertension Chronic Relapsing Cirrhosis Severe Relapsing episodes of encephalopathy Usually without precipitating factors Persistent Cirrhosis Severe Persistent cognitive or motor abnormalities Generally related to surgically induced shunts Minimal HE Cirrhosis Variable Asymptomatic Abnormalities revealed by neuropsychological or neurophysiologic tests In patients with portal-systemic bypass with no intrinsic hepatocellular disease Absent Large shunts Relapsing episodes and persistent abnormalities Rare disorder, secondary to congenital abnormalities, surgical shunts, or portal vein thrombosis Grade Criteria 1 Trivial lack of awareness, euphoria or anxiety, shortened attention span, impaired performance of addition (Sixty-seven percent of patients with cirrhosis may have minimal HE.) 2 Lethargy or apathy, minimal disorientation for time or place, subtle personality change, inappropriate behavior, impaired performance of subtraction 3 Somnolence to semistupor, but responsive to verbal stimuli; confusion; gross disorientation 4 Coma (unresponsive to verbal or noxious stimuli) T1WI Sequence 1H-MR spectroscopy MTR T2/FLAIR Sequence DWI MR imaging abnormalities Bilateral, symmetric high signal intensity of the globus pallidus and substantia nigra Increase in glutamine/glutamate signal; depletion of myo-inositol signal; decrease in choline signal; normal NAA signal Mild (10%) and diffuse decrease in normal-appearing white matter Diffuse white matter high signal intensities involving predominantly the hemispheric corticospinal tract; focal high-signal T2 lesions in subcortical hemispheric white matter Increase mean diffusivity in hemispheric white matter; normal fractional anisotropy Pathogenesis Increased brain tissue concentration of manganese Osmolar adaptation of intra-astrocytic accumulation of glutamine Mild and diffuse brain edema Mild and diffuse brain edema Interstitial brain edema Functional consequences Parkinsonism (particularly if substantia nigra is involved) Overt hepatic encephalopathy (particularly with increase in glutamine/glutamate) Functional abnormalities of the corticospinal tract on TMS Functional abnormalities of the corticospinal tract on TMS; cognitive impairment Cognitive impairment Note:—T1WI Indicates T1-weighted imaging; NAA, N-acetylaspartate; TMS, transcranial magnetic stimulation; FLAIR, fluid-attenuated inversion recovery; DWI, diffusion-weighted imaging; MTR, magnetization transfer ratio.
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