Portal-systemic encephalopathy: presence of basal ganglia lesions with high signal intensity on MR images.

Abstract

Sixteen patients with cirrhosis of the liver underwent cranial magnetic resonance (MR) imaging and transarterial portography to evaluate the relationship between basal ganglia lesions and portal-systemic collateral vessels. No neuropsychiatric disturbance was observed in any of the patients at the time of the MR examination, but four patients with portal-systemic encephalopathy were included in the study. Basal ganglia lesions, characterized by increased signal intensity on T1-weighted MR images, were observed in nine of the 16 patients, including the four with portal-systemic encephalopathy. These nine patients had large portal-systemic collateral vessels that were more than 10 mm in diameter. These collateral vessels were receiving blood from the superior mesenteric vein (SMV) in all nine patients. The lesions involved the globus pallidus and portions of internal capsules in a bilateral and symmetric fashion and did not exhibit mass effect. The authors conclude that there may be a significant relationship between high-intensity basal ganglia lesions and large portal-systemic collateral vessels receiving blood from the SMV.

Contribution of metals to brain MR signal intensity: review articles

“…Manganese is considered to be the cause of hyperintense globus pallidus in patients with chronic hepatic failure, but copper and iron as well as manganese concentrations are elevated in the globus pallidus of autopsy cases [42]. 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.…”

Nutrition in the Management of Cirrhosis and its Neurological Complications

“…Total body manganese stores are increased in patients with liver disease, 62,63 which may lead to selective manganese accumulation in several areas of the brain. [64][65][66] Manganese deposition in basal ganglia structures of the brain has been proposed as the cause of T1-weighted magnetic resonance signal hyperintensities 65 and cirrhosisrelated Parkinsonism.…”

Reprint of: Nutrition in the Management of Cirrhosis and its Neurological Complications

“…It was recently shown that selenium deficiency was also related to the severity of hepatic fibrosis in patients with hepatitis C-related chronic liver disease being one of the factors contributing to insulin resistance in these patients. 61 Manganese Total body manganese stores are increased in patients with liver disease, 62,63 which may lead to selective manganese accumulation in several areas of the brain. [64][65][66] Manganese deposition in basal ganglia structures of the brain has been proposed as the cause of T1-weighted magnetic resonance signal hyperintensities 65 and cirrhosisrelated Parkinsonism.…”