[20, 21] The cumulated numbers indicate that OHE will occur in 30%-40% of those with cirrhosis at some time during their clinical course and in the survivors in most cases repeatedly.[22] Minimal HE (MHE) or covert HE (CHE) occurs in 20%-80% of patients with cirrhosis.[23-27, 81] The prevalence of HE in prehepatic noncirrhotic portal hypertension (PH) is not well defined. The risk for the first bout of OHE is 5%-25% within 5 years after cirrhosis learn more diagnosis, depending on the presence of risk factors, such as other complications to cirrhosis (MHE or CHE,

infections, VB, or ascites) and probably diabetes and hepatitis C.[28-32] Subjects with a previous bout of OHE were found to have a 40% cumulative risk of recurring OHE at 1 year,[33] and subjects with recurrent OHE have a 40% cumulative risk of another recurrence within

6 months, despite lactulose treatment. Even individuals with cirrhosis and only mild cognitive dysfunction or mild electroencephalography (EEG) slowing develop approximately one bout of OHE per 3 years of survival.[34, PARP inhibitor 35] After TIPS, the median cumulative 1-year incidence of OHE is 10%-50%[36, 37] and is greatly influenced by the patient selection criteria adopted.[38] Comparable data were obtained by PSS surgery.[39] It gives an idea of the frequent confrontation of the health care system by patients with HE that they accounted for approximately 110,000 hospitalizations yearly (2005-2009)[40] in the United States. Though numbers in the European Union (EU) are not readily available, these predictions are expected to be similar. Furthermore, the burden of CLD and cirrhosis is rapidly increasing,[41, 42] and more cases will likely be encountered to further define the epidemiology of HE. Hepatic encephalopathy produces a wide spectrum

of nonspecific neurological and psychiatric manifestations.[10] In its lowest expression,[43, 44] HE alters only psychometric tests oriented toward attention, working MCE公司 memory (WM), psychomotor speed, and visuospatial ability, as well as electrophysiological and other functional brain measures.[45, 46] As HE progresses, personality changes, such as apathy, irritability, and disinhibition, may be reported by the patient’s relatives,[47] and obvious alterations in consciousness and motor function occur. Disturbances of the sleep-wake cycle with excessive daytime sleepiness are frequent,[48] whereas complete reversal of the sleep-wake cycle is less consistently observed.[49, 50] Patients may develop progressive disorientation to time and space, inappropriate behavior, and acute confusional state with agitation or somnolence, stupor, and, finally, coma.