Manganese intoxication and chronic liver failure are associated with strikingly similar clinical, imaging, and pathological abnormalities. As manganese is primarily cleared by the liver, inadequate elimination of manganese absorbed from the normal diet may lead to manganese overload in patients with liver disease. We report a significant elevation of blood manganese concentration in 3 patients with biopsy-proved hepatic cirrhosis who exhibited neurological dysfunction and characteristic abnormal signal hyperintensity in the globi pallidi and substantia nigra on T1-weighted magnetic resonance imaging. We speculate that manganese accumulation in the brain accounts for the magnetic resonance imaging abnormalities and contributes to neurological dysfunction in patients with liver disease.

BACKGROUND AND PURPOSE:As the standard of care for the evaluation of the cervical spine shifts from plain radiographs to multidetector row CT (MDCT), a re-examination of the normal anatomic relationships of the occipitovertebral articulations is needed. We aimed to define the normal anatomic relationships of craniocervical articulations on MDCT and address any discrepancies with currently accepted ranges of normal on plain radiographs.

Background: Chronic liver failure is associated with high signal abnormalities in the basal ganglia on Tl-weighted magnetic resonance imaging of the brain. These abnormalities are strikingly similar to those seen following manganese intoxication. As dietary manganese is normally cleared by the liver, we hypothesize that hepatic dysfunction could lead to manganese overload and account for the MR1 abnormalities seen in patients with chronic liver disease. Methods: We measured blood manganese concentrations in eleven patients with biopsy-proven hepatic cirrhosis and eleven healthy age and sex-matched controls. We also performed semi-quantitative measures of Tl signal abnormalities on MRI in the patients with chronic liver disease. Results: Patients with cirrhosis had significantly higher blood manganese concentrations (20.6 ± 10.2 mcg/L) than controls (7.2 ± 2.7, p = .0013). In addition, semi-quantitative scores of TI-weighted signal hyperintensity on MRI correlated with blood manganese concentration in patients with cirrhosis (r = .65, p = .029). Conclusions: These findings demonstrate that chronic liver disease is associated with manganese overload and suggest that manganese is responsible for the Tlweighted signal hyperintensity seen on MRI of patients with liver disease. As manganese intoxication is known to cause parkinsonism and an encephalopathy similar to those which occur with chronic liver disease, it is possible that manganese toxicity contributes to the development of these symptoms in liver damaged patients and that therapies which prevent or reduce manganese overload may have clinical benefit. RESUME: Le taux de manganese sanguin est en correlation avec les changements observes a I'imagerie par resonance magnetique chez les patients avec atteinte hepatique. Introduction: L'insuffisance hdpatique chronique est associde a des anomalies du signal dans le noyau lenticulaire, le noyau caudd, I'avant-mur et le noyau amygdalien a I'imagerie par resonance magndtique avec ponddration Tl du cerveau. Ces anomalies sont dtonnammant semblables a celles observdes dans l'intoxication au manganese. Comme le manganese de la diete est normalement dlimind par le foie, nous avons dmis l'hypothese qu'une dysfonction hdpatique pourrait engendrer une surcharge en manganese et etre responsable des anomalies observdes a I'IRM chez les patients atteints de maladie hdpatique chronique. Methodes: Nous avons mesurd la concentration de manganese sanguin chez onze patients avec cirrhose hdpatique prouvde par biopsie et onze controles sains, apparids pour I'Sge et le sexe. Nous avons dgalement rdalisd des mesures semi-quantitatives des anomalies de signal Tl a I'IRM chez les patients atteints de maladie hdpatique chronique. Rdsultats: Les patients atteints de cirrhose avaient des concentrations sanguines de manganese significativement plus dlevdes (20.6 ± 10.2 mcg/L) que les controles (7.2 ± 2.7, p=.0013). De plus, les scores semi-quantitatifs de l'hyperintensitd du signal ponddrd Tl a I'IRM etaient corrdlds avec les conce...

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