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Hepatic encephalopathy (HE) is a common complication of cirrhosis that is associated with brain atrophy and may participate in impaired cognitive function after liver transplantation. This study analyzes the relationship of HE with cognitive function and brain volume after transplantation. A total of 52 consecutive patients with cirrhosis (24 alcohol abuse, 24 prior HE, 14 diabetes mellitus) completed a neuropsychological assessment before liver transplantation and again, 6 to 12 months after transplantation. In 24 patients who underwent the posttransplant assessment, magnetic resonance imaging was performed in addition, with measurement of brain volume and relative concentration of N-acetylaspartate (NAA) and creatine/ phosphocreatine (Cr), a neuronal marker, by magnetic resonance spectroscopy. Neuropsychological assessment prior to transplantation identified minimal HE in 28 patients. All cognitive indexes improved after liver transplantation, but 7 patients (13%) showed persistent mild cognitive impairment. Global cognitive function after transplantation was poorer in patients with the following variables before liver transplantation: alcohol etiology, diabetes mellitus, and HE. Brain volume after transplantation was smaller in patients with prior HE. Brain volume correlated to NAA/Cr values (r ¼ 0.498, P ¼ 0.013) and poor motor function (r ¼ 0.41, P ¼ 0.049). In conclusion, the association of HE with cognitive function and brain volume suggests that having experienced HE before liver transplantation impairs the posttransplantation neurological outcome. Liver Liver transplant candidates often exhibit cognitive disturbances, which are related to the effects of liver failure, the etiology of liver disease (eg, alcoholism), complications of cirrhosis (eg, hyponatremia), and extrahepatic comorbidities (eg, cerebrovascular disease). 1 The most common cause of cognitive impairment appears to be minimal hepatic encephalopathy (HE), which is secondary to liver failure and shares the same pathogenic mechanism as overt HE. Liver transplantation (LT) restores liver function and results in an improvement of minimal HE. 2 However, it is unclear whether minimal HE is fully reversible or

Diet supplementation with BCAA after an episode of HE does not decrease recurrence of HE. However, supplementation with BCAA improves minimal HE and muscle mass. Identification of risk factors for recurrence of HE may allow the development of new preventive therapies that could decrease the neuropsychological sequelae of repeated episodes of HE.

Several clinical variables, potentially treatable, may alter particular aspects of HRQOL. Correction of ascites, hypoalbuminemia, minimal hepatic encephalopathy, and anemia may cause a positive impact on HRQOL of patients with cirrhosis.

Focal T2-weighted white matter lesions (WML) on brain magnetic resonance imaging (MRI), mimicking those seen in cerebrovascular small-vessel disease described in patients with persistent hepatic encephalopathy, decreased in volume with the improvement of hepatic encephalopathy. This outcome has been interpreted as a decrease in the edema that it is proposed to be involved in the pathogenesis of hepatic encephalopathy. We designed a study to further investigate potential changes in focal WML in the brains of patients with cirrhosis following liver transplantation and to study the relationship between these changes and overall cognitive function. We used MRI to measure the volume of supratentorial focal WML and a neuropsychological examination to assess cognitive function before and after liver transplantation in 27 patients with cirrhosis without signs of overt hepatic encephalopathy. Baseline MRI identified focal T2-weighted lesions in 19 patients (70.3%). The presence of WML was associated with older age but not with vascular risk factors, severity of liver function, or psychometric tests. A significant reduction in lesion volume was observed after liver transplantation (from a median of 1.306 cm 3 to 0.671 cm 3 , P ‫؍‬ 0.001). This decrease correlated with an improvement in an index of global cognitive function (r ‫؍‬ ؊0.663; P < 0.001). This evolution indicates that lesion volume is partially related to a reversible type of tissue damage, which is compatible with brain edema. F ocal white matter lesions (WML) secondary to cerebrovascular small-vessel disease are commonly found in the general population over 60 years of age. 1 In a previous report, we described focal brain WML on T2-weighted images in patients with hepatic encephalopathy (HE). 2 This abnormality, which is radiologically indistinguishable from the features of small-vessel disease or normal aging, was partially reversible with improvements in HE. This evolution pattern contrasts with what occurs in focal WML attributable to small-vessel disease or brain aging, which remain stable or progress in number and size over time, but never decrease. [3][4][5] The most plausible explanation for decreasing the volume of WML with improvement of HE is a decrease in the edema component of WML.There is a large body of evidence indicating an increase in the amount of water in the brain of patients with liver cirrhosis that is related to the development of HE. 6 The most accepted hypothesis for this low-grade brain edema is that astrocytic accumulation of glutamine induces edema as a result of ammonia detoxification. This hypothesis is supported by experimental data showing astrocyte swelling and changes in brain organic osmolytes in models of HE, 7 and by brain proton magnetic resonance spectroscopy studies in patients with liver cirrhosis, which consistently show increases in the glutamine/glutamate signal accompanied by myoinositol depletion, 8

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