1H magnetic resonance (1H MR) studies of the brain in patients with liver diseases have shown several abnormalities that may be relevant for the pathogenesis of hepatic encephalopathy. 1H magnetic resonance imaging shows a typical pallidal hyperintensity on T1-weighted images. This abnormality appears to be secondary to the accumulation of manganese in basal ganglia because of portal-systemic shunting. No direct correlation between the magnitude of pallidal hyperintensity and the grade of hepatic encephalopathy has been found, but some studies have related pallidal hyperintensity to parkinsonism. 1H magnetic resonance spectroscopy shows relative to creatine an increase in glutamine/glutamate (Glx) signal and a decrease of choline containing compounds (Cho) and myo-inositol. Abnormalities in the Glx signal have been interpreted as an increase in brain glutamine secondary to the metabolism of ammonia in astrocytes. Disturbances of Cho and myo-inositol have been interpreted as a compensatory response to the increase in intracellular osmolality caused by the accumulation of glutamine in astrocytes. In addition, magnetization transfer imaging shows signs compatible with low-grade cerebral edema. Altogether, 1H MR studies suggest the accumulation of manganese and the development of osmotic abnormalities in the brain of patients with cirrhosis. These abnormalities appear to participate in some of the neurological manifestations of hepatic encephalopathy.
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