Liver cirrhosis is an increasing public health threat worldwide. Malnutrition is a serious complication of cirrhosis and is associated with worse outcomes. With this review, we aim to describe the prevalence of malnutrition, pathophysiological mechanisms, diagnostic tools and therapeutic targets to treat malnutrition. Malnutrition is frequently underdiagnosed and occurs—depending on the screening methods used and patient populations studied—in 5–92% of patients. Decreased energy and protein intake, inflammation, malabsorption, altered nutrient metabolism, hypermetabolism, hormonal disturbances and gut microbiome dysbiosis can contribute to malnutrition. The stepwise diagnostic approach includes a rapid prescreen, the use of a specific screening tool, such as the Royal Free Hospital Nutritional Prioritizing Tool and a nutritional assessment by dieticians. General dietary measures—especially the timing of meals—oral nutritional supplements, micronutrient supplementation and the role of amino acids are discussed. In summary malnutrition in cirrhosis is common and needs more attention by health care professionals involved in the care of patients with cirrhosis. Screening and assessment for malnutrition should be carried out regularly in cirrhotic patients, ideally by a multidisciplinary team. Further research is needed to better clarify pathogenic mechanisms such as the role of the gut-liver-axis and to develop targeted therapeutic strategies.

Items located within an array were presented to alcoholic Korsakoff and nonalcoholic mixed-etiology amnesics and to alcoholic and normal controls. Recognition memory for the locations of items was tested after incidental and intentional encoding. When equated on item recognition, neither Korsakoff amnesics nor alcoholic controls benefited from intentional, relative to incidental, encoding instructions. Furthermore, Korsakoff amnesics showed neither disproportionately impaired incidental nor intentional location recognition memory relative to alcoholic controls. In contrast, mixed-etiology amnesics profited significantly from intentional location acquisition relative to incidental instructions, and were impaired somewhat in incidental, but not intentional, location memory relative to normal controls. We discuss these data in relation to Mayes' (1992) contextual memory deficit hypothesis and Hirst's (1982) automatic encoding deficit account, and propose an alternative framework in which the location memory deficit observed in mixed-etiology amnesics is interpreted as a disruption to the ability to bind item and location information.

To assess if amnesics have intact remote memory for general semantic information, we examined memory for vocabulary words with known dates of entry into the language between 1955 and 1989. Amnesics of mixed etiology with acute onset performed normally on both a recall and a recognition task. Korsakoff patients, in contrast, were impaired on both tasks and demonstrated a gradient such that their knowledge of words acquired during more recent time periods was worse than that of words acquired during more remote time periods. The improvement in performance associated with recognition testing was larger for Korsakoff patients than for control subjects and correlated significantly with a composite measure of frontal dysfunction. These findings suggest a deficit in the controlled search and retrieval of semantic information in Korsakoff patients. The implications of the differential performance of Korsakoff and mixed etiology amnesics for explanations of temporally graded retrograde amnesia are discussed. (JINS, 1995, I, 443–453.)

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