Induced hyperammonaemia may compromise the ability to generate restful sleep in patients with cirrhosis

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http://onlinelibrary.wiley.com/doi/10.1002/hep.24741/abstract

Liver Failure, Cirrhosis and Portal Hypertension

Induced hyperammonaemia may compromise the ability to generate restful sleep in

patients with cirrhosis

A Bersagliere1,2,†, ID Raduazzo3,†, M Nardi3, S Schiff3, A Gatta3, P Amodio3, P

Achermann1,2,4,‡, S Montagnese3,*,

‡DOI: 10.1002/hep.24741

Copyright © 2011 American Association for the Study of Liver Diseases

Issue

Hepatology

Accepted Article (Accepted, unedited articles published online for future

issues)

Abstract

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.)