Bright basal ganglia in T1-weighted magnetic resonance images are frequent in patients with portal vein thrombosis without liver cirrhosis and not suggestive of hepatic encephalopathy
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Cited by (47)
Laboratory Abnormalities of Hepatic Encephalopathy
2020, Clinics in Liver DiseaseCitation Excerpt :One study could not find a statistically significant correlation between globus pallidus signals in T1W images with chronic HE.28 Another study demonstrated that basal ganglia hyperintensity represents shunt-induced alterations including portal vein thrombosis and cavernous transformation without signs of liver disease, rather than altered liver function or HE.29 Fukuzawa and colleagues30 showed that pallidal hyperintensity on MRI was more prominent in patients with idiopathic portal hypertension than in those with liver cirrhosis, and there was no correlation between hyperintensity and severity of liver dysfunction or HE; there was a stronger correlation with portosystemic shunt in portal hypertension than liver cirrhosis.
Clinical and Neurologic Manifestation of Minimal Hepatic Encephalopathy and Overt Hepatic Encephalopathy
2015, Clinics in Liver DiseaseBrain magnetic resonance in hepatic encephalopathy
2014, Seminars in Ultrasound, CT and MRICitation Excerpt :Subsequent MR studies show that restoration of liver function can slowly reverse this signal abnormality15,17-21 (Fig. 1). This hyperintensity has also been observed in patients with noncirrhotic portal vein thrombosis who did not have overt HE.22 Nevertheless, patients showing impairment on neuropsychological tests similar to that described in MHE exhibit higher pallidal intensity than patients with normal neuropsychological function.23-25
Manganese and the Brain
2013, International Review of NeurobiologyCitation Excerpt :AHD seems to occur in any type of chronic liver disease; however, the presence of portosystemic shunting in addition to hepatocellular dysfunction seems to be a prerequisite for Mn accumulation (Burkhard et al., 2003; Butterworth, 2012; Rose et al., 1999). In rare cases, portosystemic shunts without hepatocellular dysfunction such as hereditary hemorrhagic telangiectasias or portal vein thrombosis have been reported to cause Mn toxicity and AHD (Kumar et al., 2008; Nolte et al., 1998). While the majority of cases of AHD have been described in the adult population, AHD can also be a complication of end-stage liver disease in children (Bekiesinska-Figatowska, Mierzewska, & Jurkiewicz, 2013; Papapetropoulos et al., 2008; Pinto et al., 2010).
Chronic hepatic encephalopathy in a patient with primary biliary cirrhosis
2011, Gastroenterologia y Hepatologia