Sleep disturbance and daytime sleepiness in patients with cirrhosis: a case control study

Mostacci, Barbara; Ferlisi, Monica; Antognini, Alessandro Baldi; Sama, C; Morelli, Cristina; Mondini, Susanna; Cirignotta, Fabio

doi:10.1007/s10072-008-0973-7

Cited by 79 publications

(82 citation statements)

References 24 publications

(23 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Sleep disturbance is seen in 26-70% of patients with cirrhosis. [52][53][54][55][56] Studies have confirmed higher frequency of sleep disturbances in patients of cirrhosis with MHE compared to those without MHE. 11,52 Sleep is maintained by two processes namely, 'Homeostatic process' that determines sleep propensity in relation to waking hours and 'Circadian process' under the control of suprachiasmatic nucleus and its retino-hypothalamic axis which responds to light-dark cues by melatonin secretion.…”

Section: Sleep and Health Related Quality Of Lifementioning

confidence: 97%

Minimal Hepatic Encephalopathy Impairs Quality of Life

Agrawal

Umapathy

Dhiman

2015

Journal of Clinical and Experimental Hepatology

View full text Add to dashboard Cite

Minimal hepatic encephalopathy (MHE) is the mildest form of the spectrum of neurocognitive impairment in cirrhosis. It is a frequent occurrence in patients of cirrhosis and is detectable only by specialized neurocognitive testing. MHE is a clinically significant disorder which impairs daily functioning, driving performance, work capability and learning ability. It also predisposes to the development of overt hepatic encephalopathy, increased falls and increased mortality. This results in impaired quality of life for the patient as well as significant social and economic burden for health providers and care givers. Early detection and treatment of MHE with ammonia lowering therapy can reverse MHE and improve quality of life. ( J CLIN EXP HEPATOL 2015;5:S42-S48) H epatic encephalopathy (HE) is a neurocognitive disorder in which brain function is impaired and is associated with both acute and chronic liver dysfunction. 1 It is a major complication that develops in some form and at some stage in a majority of patients with liver cirrhosis. Minimal HE (MHE) is the mildest form of spectrum of HE which is characterized by subtle cognitive and psychomotor deficits in the absence of recognizable clinical symptoms of HE. 2 It occurs in patients with liver dysfunction and/or portosystemic shunts. In MHE, neurocognitive abnormalities primarily affect attention, speed of information processing, executive control, motor ability and coordination in an individual. 3 In 1970, Zeegen et al 4 first described this condition when they discovered that 38% of patients who had undergone portal decompression surgery scored abnormal in Reitan trail making test (number connection test). Eight years later, the term subclinical HE 5 was introduced to describe these patients. Since then, this condition was described under various names like early HE, latent HE, subclinical HE and finally minimal HE. The latest classification combines MHE and grade 1 HE into covert HE while higher grades are classified as overt HE, thus simplifying the clinical schema so that HE can be uniformly diagnosed. 6 Covert HE means that the mental defect is not detectable by the clinician using conventional testing and is not noticeable to the patient. However, it is significant because these patients usually have neuropsychiatric and neurophysiological abnormalities on advanced testing which are not enough to cause disorientation or asterixis. MHE is regarded as a preclinical stage of HE and ammonia and systemic inflammation plays an important role in its pathogenesis similar to HE. Ammonia lowering therapies were used in the treatment of MHE and found to be effective.MHE is clinically significant as it impairs daily functioning, health related quality of life (HRQOL) and driving skills, predicts the development of overt HE and is associated with poor survival. 7-11 Overt HE develops in >50% of MHE patients within three years. 10 These patients pose a significant burden to their care givers depending on the severity of cognitive dysfunction. 2,12 Considering all ...

show abstract

Section: Sleep and Health Related Quality Of Lifementioning

confidence: 97%

Minimal Hepatic Encephalopathy Impairs Quality of Life

Agrawal

Umapathy

Dhiman

2015

Journal of Clinical and Experimental Hepatology

View full text Add to dashboard Cite

show abstract

“…While there is evidence for this in animal models, human studies provide a considerably more heterogeneous picture. [22][23][24][25][26] This may be due to a number of factors, including cultural and environmental confounders, the heterogeneity of the patient populations studied, and a certain tendency of hepato-gastroenterologists and internists to group all kinds of sleep disturbances together, and to study them with tools such as quality of life and psychological well-being questionnaires. 23 In more recent years, some work has been devoted to defining the sleepwake disturbances exhibited by these patients in a more formal, systematic fashion, in collaboration with sleep scientists and chronobiologists.…”

Section: Sleepiness and Hepatic Encephalopathymentioning

confidence: 99%

“…19 In at least two studies, an association between excessive sleepiness and the presence/degree of HE was also observed. [24][25][26] In addition, sleepiness has been shown to be more common in cirrhotic patients with a history of HE and documented portal-systemic shunt, 28 and to be positively correlated with the amount of slow activity on the wake EEG. 24 This is a well-established marker of HE, 29 and one of the neurophysiological correlates of sleepiness.…”

Section: Sleepiness and Hepatic Encephalopathymentioning

confidence: 99%

Hepatic Encephalopathy and Sleepiness: An Interesting Connection?

Montagnese

Turco

Amodio

2015

Journal of Clinical and Experimental Hepatology

View full text Add to dashboard Cite

Sleep-wake abnormalities in patients with cirrhosis have been traditionally associated with hepatic encephalopathy (HE). In recent years, a certain amount of work has been devoted to the study of this relationship. This has lead to a modified picture, with weakening of the association between HE and poor night sleep, and the emergence of stronger links between HE and excessive daytime sleepiness. This brief review focuses on the evidence in favor of the interpretation of HE as a sleepiness syndrome, and on the diagnostic, therapeutic and social implications of such an interpretation. ( J CLIN EXP HEPATOL 2015;5:S49-S53) S leepiness is the expression of a basic physiological need, not unlike hunger or thirst. 1 Its presence and its intensity can be indirectly measured by how readily sleep occurs, how easily it is disrupted, and how long it lasts. Sleep deprivation/restriction increase sleepiness, and sleep reverses it. Routine access to sleep, not unlike that to food or drink, is not only homeostatic, but is influenced by social and environmental factors. Thus subjective sleepiness and its indicators (yawning, nodding etc.) are reduced under conditions such as social interaction, exercise etc. 2 However, when sleepiness is severe, our ability to reduce its impact on behavior is reduced, and the likelihood of sleep increases. There is probably some degree of adaptation to chronic sleepiness, and successfully treated patients report that "they had forgotten the experience of complete alertness". 2 This could provide an explanation for our observation that induced hyperammonaemia results in significantly more pronounced subjective sleepiness in healthy volunteers compared to cirrhotic patients, who may be used to it. 3 The degree of daytime sleepiness is related to both the amount of nocturnal sleep (sleep deprivation/restriction results in increased sleepiness during the following day, 4 ) and its quality (night arousals of different etiology, fragmenting sleep, also result in increased daytime sleepiness. 5 ) Finally, there is a circadian element to sleepiness. Subjects who are allowed to nap in time-free environments do so in a biphasic pattern, with a nap in the middle of the 24-h cycle (or early in the afternoon). 6 Such rhythmicity is preserved in "jet-lagged" conditions, just like that of sleep and feeding.It is assumed that sleepiness is a central nervous system phenomenon with identifiable neural mechanisms. However, limited information is available on whether: 1) the neurochemistry of sleepiness is different to that of sleep; 2) sleepiness and alertness have common or separate neural and neurochemical correlates. The electroencephalogram (EEG) of behaviorally awake subjects who have been deprived/restricted of sleep documents microsleep episodes and increased amounts of theta activity. 7 These neurophysiological events are considered markers/correlates of sleepiness. Neurophysiological studies have implicated histamine, serotonin, catecholamines, and acetylcholine in the control of wakefulness, and gamm...

show abstract

“…Sleep disturbances were reported in subjects with cirrhosis [4,12,13]; daily somnolence is the one that has a proven relationship with HE [14]. Finally, it was recently recognized that HE is associated with falls; if this is caused by cognitive or motor abnormalities or by their combination, or even by cirrhosis per se, is not yet clear [15,16].…”

Section: Clinical Manifestationmentioning

confidence: 99%

Hepatic encephalopathy

Amodio¹

2015

Cirrhosis: A Practical Guide to Management

View full text Add to dashboard Cite

Sleep disturbance and daytime sleepiness in patients with cirrhosis: a case control study

Cited by 79 publications

References 24 publications

Minimal Hepatic Encephalopathy Impairs Quality of Life

Minimal Hepatic Encephalopathy Impairs Quality of Life

Hepatic Encephalopathy and Sleepiness: An Interesting Connection?

Hepatic encephalopathy

Contact Info

Product

Resources

About