Increasing evidence suggests that
manganese deposition is responsible for the T1-weighted magnetic resonance imaging (MRI) signal hyperintensity consistently observed in pallidum of cirrhotic patients. However, the relationship between blood
manganese and the etiology or severity of
liver disease, as well as the neurological symptomatology in these patients, has not been well established. In the present study, blood
manganese concentrations were measured by atomic absorption spectrometry together with MRI and neurological evaluation in 57 cirrhotic patients with various etiologies and severity of
liver disease. Blood
manganese concentrations were elevated in 67% of cirrhotic patients and were significantly higher in patients with previous
portacaval anastomoses or transjugular intrahepatic
portosystemic shunt (
TIPS). Pallidal signal hyperintensity was observed in 88% of patients, and significant correlations were demonstrated between blood
manganese and pallidal index (PI) (a measure of pallidal signal hyperintensity), as well as Child-Pugh score. Assessment of extrapyramidal symptoms using the Columbia rating scale revealed a significant incidence of
tremor, rigidity, or akinesia in up to 89% of cirrhotic patients. However, there was no significant correlation between blood
manganese and extrapyramidal symptoms, although severity of akinesia was significantly greater in Child-Pugh C patients. Extrapyramidal symptoms could result from a toxic effect of
manganese on basal ganglia dopaminergic function. These findings further support a role for
manganese in the etiology of pallidal MRI signal hyperintensity in patients with chronic
liver disease.