MRI findings in chronic hepatic encephalopathy depend on portosystemic shunt: results of a controlled prospective clinical investigation

Krieger, Silke; Jauß, M.; Jansen, Olav; Stiehl, A.; Sauer, Peter; Geissler, M; Theilmann, Lorenz; Krieger, Derk

doi:10.1016/s0168-8278(97)80290-5

Cited by 55 publications

(33 citation statements)

References 17 publications

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“…5 Furthermore, T1-weighted MR signal intensity in pallidum significantly increased after transjugular portosystemic shunt placement but not after elective sclerotherapy in similar patients. 25 Pallidal signal hyperintensity 26 on MRI was previously reported in a child with patent ductus venosus in the absence of significant liver disease.…”

Section: Discussionmentioning

confidence: 84%

Manganese deposition in basal ganglia structures results from both portal-systemic shunting and liver dysfunction

et al. 1999

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Background & Aims: Manganese (Mn) deposition could be responsible for the T1-weighted magnetic resonance signal hyperintensities observed in cirrhotic patients. These experiments were designed to assess the regional specificity of the Mn increases as well as their relationship to portal-systemic shunting or hepatobiliary dysfunction. Methods: Mn concentrations were measured in (1) brain samples from basal ganglia structures (pallidum, putamen, caudate nucleus) and cerebral cortical structures (frontal, occipital cortex) obtained at autopsy from 12 cirrhotic patients who died in hepatic coma and from 12 matched controls; and from (2) brain samples (caudate/putamen, globus pallidus, frontal cortex) from groups (n = 8) of rats either with end-to-side portacaval anastomosis, with biliary cirrhosis, or with fulminant hepatic failure as well as from sham-operated and normal rats. Results: Mn content was significantly increased in frontal cortex (by 38%), occipital cortex (by 55%), pallidum (by 186%), putamen (by 66%), and caudate (by 54%) of cirrhotic patients compared with controls. Brain Mn content did not correlate with patient age, etiology of cirrhosis, or history of chronic hepatic encephalopathy. In cirrhotic and portacaval-shunted rats, Mn content was increased in pallidum (by 27% and 57%, respectively) and in caudate/putamen (by 57% and 67%, respectively) compared with control groups. Mn concentration in pallidum was significantly higher in portacaval-shunted rats than in cirrhotic rats. No significant changes in brain Mn concentrations were observed in rats with acute liver failure. Conclusions: These findings suggest that brain Mn deposition results both from portal-systemic shunting and from liver dysfunction.

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Section: Discussionmentioning

confidence: 84%

Manganese deposition in basal ganglia structures results from both portal-systemic shunting and liver dysfunction

et al. 1999

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“…The hyperintense globus pallidus seen in hepatic failure occurs due to an elevated concentration of manganese in the blood, which passes through the portal-systemic collateral vessels without migrating through the liver [43]. The hyperintense globus pallidus observed in schistosomiasis [44], Osler-Weber-Rendu disease [45], and post-transjugular intrahepatic portosystemic shunt placement [46] is also considered to be related to portalsystemic shunting. On the other hand, a hyperintense globus pallidus sometimes develops in patients with chronic liver failure in the absence of portal-systemic shunting [47].…”

Section: Manganesementioning

confidence: 99%

Contribution of metals to brain MR signal intensity: review articles

et al. 2016

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“…We previously observed significant correlations between blood manganese, pallidal hyperintensity and the presence of portal-systemic shunting in cirrhotic patients (Spahr et al, 1996). A significant increase of pallidal hyperintensity has been reported to occur after TIPS (Krieger et al, 1997). Typical pallidal images were also described in a patient with patent ductus venosus (spontaneous portocaval shunt) in the absence of liver disease (Yanai et al, 1995) and in 6 patients with portal vein thrombosis, portal-systemic collaterals and a normal liver (Nolte et al, 1998).…”

Section: Relationship Between Brain Manganese Deposition and Chronic mentioning

confidence: 85%

“…Accordingly it has been demonstrated that, several months after liver transplantation, neurological dysfunction improved or normalised and that MR pallidal hyperintensity disappeared (Devenyi et al, 1994, Pujol et al, 1993. More recently, it has been shown that, after the placement of an intrahepatic shunt, pallidal hyperintensity and neurological impairment worsened in a population of cirrhotic patients treated with this procedure compared to a control group (Krieger et al, 1997).…”

Section: Relationship Between Brain Manganese Accumulation and Neurolmentioning

confidence: 99%

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Layrargues

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Spahr

et al. 1998

Metabolic Brain Disease

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Amongst the potential neurotoxins implicated in the pathogenesis of hepatic encephalopathy, manganese emerges as a new candidate. In patients with chronic liver diseases, manganese accumulates in blood and brain leading to pallidal signal hyperintensity on T1-weighted Magnetic Resonance (MR) Imaging. Direct measurements in globus pallidus obtained at autopsy from cirrhotic patients who died in hepatic coma reveal 2 to 7-fold increases of manganese concentration. The intensity of pallidal MR images correlates with blood manganese and with the presence of extrapyramidal symptoms occurring in a majority of cirrhotic patients. Liver transplantation results in normalization of pallidal MR signals and disappearance of extrapyramidal symptoms whereas transjugular intrahepatic portosystemic shunting induces an increase in pallidal hyperintensity with a concomitant deterioration of neurological dysfunction. These findings suggest that the toxic effects of manganese contribute to extrapyramidal symptoms in patients with chronic liver disease. The mechanisms of manganese neurotoxicity are still speculative, but there is evidence to suggest that manganese deposition in the pallidum may lead to dopaminergic dysfunction. Future studies should be aimed at evaluating the effects of manganese chelation and/or of treatment of the dopaminergic deficit on neurological symptomatology in these patients.

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MRI findings in chronic hepatic encephalopathy depend on portosystemic shunt: results of a controlled prospective clinical investigation

Cited by 55 publications

References 17 publications

Manganese deposition in basal ganglia structures results from both portal-systemic shunting and liver dysfunction

Manganese deposition in basal ganglia structures results from both portal-systemic shunting and liver dysfunction

Contribution of metals to brain MR signal intensity: review articles

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