In patients with cirrhosis, hyperammonaemia and hepatic encephalopathy are common after a gastrointestinal bleeding and can be simulated by an amino acid challenge (AAC), or the administration of a mixture of amino acids mimicking the composition of haemoglobin. The aim of this study was to investigate the clinical, psychometric, wake-/sleep-EEG correlates of induced hyperammonaemia. Ten patients with cirrhosis and ten matched healthy volunteers underwent: i) 8-day sleep quality/timing monitoring; ii) neuropsychiatric assessment at baseline/after AAC; iii) hourly ammonia/subjective sleepiness assessment for 8 hours after AAC; iv) sleep EEG recordings (nap opportunity: 17:00-19:00) at baseline/after AAC. Neuropsychiatric performance was scored according to age-/education-adjusted Italian norms. Sleep stages were scored visually for 20-s epochs; power density spectra were calculated for consecutive 20-s epochs and average spectra determined for consolidated episodes of nonREM sleep of minimal common length. The AAC resulted in: i) an increase in ammonia concentrations/subjective sleepiness in both patients and healthy volunteers; ii) a worsening of neuropsychiatric performance (wake EEG slowing) in two (20%) patients and none of the healthy volunteers; iii) an increase in the length of nonREM sleep in healthy controls [49.3(26.6) vs. 30.4(15.6) min; p=0.08]; iv) a decrease in the sleep EEG beta power (fast activity) in the healthy volunteers; v) a decrease in the sleep EEG delta power in patients. IN CONCLUSION: the AAC led to significant increase in daytime subjective sleepiness and changes in the EEG architecture of a subsequent sleep episode in patients with cirrhosis, pointing to a reduced ability to produce restorative sleep. (HEPATOLOGY 2011.).