Pallidal lesions in patients with liver cirrhosis: clinical and MRI evaluation

Abstract

Fifty patients with liver cirrhosis underwent neurological, psychometric, electroencephalographic and biochemical examination as well as cranial magnetic resonance imaging (MRI) to study the incidence of pallidal lesions in cirrhotics and their correlation to liver function, as well as to neurological and mental state. In one patient a histopathological study of the brain was performed. The vast majority of the patients with liver cirrhosis (92%) present with bilateral symmetric pallidal hyperintensities in the T1-weighted MR spin echo sequence, while the T2-weighted images are normal. On the whole there was no correlation between the signal intensity of the pallidal lesions and measures of liver function, neurological status or grade of encephalopathy. As could be shown in follow-up examinations the signal intensity of the lesions increased with decreasing liver function and decreased with normalization of liver function after liver transplantation. The substrate of the lesions remains unclear. However, regions which show alterations in the MRI are histopathologically characterized by the appearance of Alzheimer-type-II cells.

Demonstration of interstitial cerebral edema with diffusion tensor MR imaging in type C hepatic encephalopathy†

“…8,13,14 Although various causes have been proposed 8,14 for this hyperintensity, deposition of manganese is regarded as the most likely explanation, 12 with no direct correlation of pallidal hyperintensity and grade of encephalopathy. 15 MT imaging has shown decreased MT ratio (MTR) in all brain regions in patients with chronic HE. 10,16 The likely explanation proposed is Alzheimer type II change and increased water content in astrocytes.…”

Minimal Hepatic Encephalopathy (MHE)

“…88 Basal ganglia T1-weighted signal intensity and manganese accumulation appear to be related to the underlying degree of portal-systemic shunting rather than directly to neuropsychiatric impairment. 90 H y p e r i n t e n s e g l o b u s p a l l i d u s o n M R I i s c o m m o n i n p a t i e n t s w i t h l i v e r cirrhosis and also occurs in patients with noncirrhotic portal hypertension.…”

Portal-Systemic Encephalopathy in Emergency Treatment of Cirrhosis and Bleeding Esophageal Varices

“…Manganese is neurotoxic, affecting both neuronal and astrocytic integrity. In the case of astrocytes, exposure to manganese results in altered expression of several key astrocytic proteins (Hazell et al, 1999a;Hazell et al, 1999b) and Alzheimer type II changes (Weissenborn et al, 1995).…”