long-term parenteral nutrition, 3 and after occupational man-Increasing evidence suggests that manganese deposiganese exposure sufficient to cause Parkinson's-like extrapytion is responsible for the T 1 -weighted magnetic resoramidal symptoms. 4 MRI signal hyperintensities may disapnance imaging (MRI) signal hyperintensity consistently pear after the cessation of manganese administration during observed in pallidum of cirrhotic patients. However, the parenteral nutrition 5 or after liver transplantation. 1 More relationship between blood manganese and the etiology recently, we demonstrated that pallidal manganese concenor severity of liver disease, as well as the neurological trations were markedly elevated in cirrhotic patients who symptomatology in these patients, has not been well esdied in hepatic coma. 6 tablished. In the present study, blood manganese con-Hepatic encephalopathy (HE) is a spectrum of neuropsychicentrations were measured by atomic absorption specatric disturbances occurring in patients with chronic liver trometry together with MRI and neurological evaluation disease. Variable degrees of impairment of mental function in 57 cirrhotic patients with various etiologies and seare observed, and close clinical examination may disclose exverity of liver disease. Blood manganese concentrations trapyramidal signs. Recent reports evaluating the relationwere elevated in 67% of cirrhotic patients and were sigship between pallidal hyperintensity and neurological sympnificantly higher in patients with previous portacaval toms provide conflicting results. [7][8][9][10][11][12] Because manganese anastomoses or transjugular intrahepatic portosystemic toxicity may result in both pallidal hyperintensity and in shunt (TIPS). Pallidal signal hyperintensity was ob-Parkinson's-like extrapyramidal symptoms, and because served in 88% of patients, and significant correlations similar symptoms have been described in patients with were demonstrated between blood manganese and palchronic liver disease, we evaluated and attempted to correlidal index (PI) (a measure of pallidal signal hyperintenlate, in the same cirrhotic patients, neurological status, T 1sity), as well as Child-Pugh score. Assessment of extrapyweighted pallidal MRI signal intensity, and blood manganese ramidal symptoms using the Columbia rating scale concentrations. revealed a significant incidence of tremor, rigidity, or akinesia in up to 89% of cirrhotic patients. However,
PATIENTS AND METHODS
there was no significant correlation between blood man-Patients. Fifty-seven patients with biopsy-proven cirrhosis were ganese and extrapyramidal symptoms, although severincluded in the present study. None of them had clinically overt ity of akinesia was significantly greater in Child-Pugh encephalopathy. Clinical and biochemical characteristics are shown C patients. Extrapyramidal symptoms could result from in Table 1. a toxic effect of manganese on basal ganglia dopaminer-Neurological evaluation was performed by the same neurologist gic function. These findings further support a role for (L.B.) who was blinded to the MRI and blood manganese data. As- manganese in the etiology of pallidal MRI signal hypersessment of extrapyramidal symptoms was made using the Columbia intensity in patients with chronic liver disease. (HEPAscale (maximum score, 76), 13 in which the following items were scored: tremor, rigidity, and degree of akinesia (evaluated from facial