Prevalence and prognostic value of quantified electroencephalogram (EEG) alterations in cirrhotic patients
Introduction
Abnormalities of the electroencephalogram (EEG) in hepatic encephalopathy have been known since 1950 when Foley et al. [1] described the slow high-voltage EEG discharges in patients with hepatic coma. The visual EEG findings in cirrhosis and their relationship to mental and neurological conditions were clearly described by Parsons-Smith et al. [2]. An objective classification of EEG alterations in hepatic encephalopathy that was based on EEG parameters obtained by automatic quantitative spectral analysis was proposed more recently by Van der Rijt et al. [3]. Such a technique increases the reliability of EEG assessment [4]. Even though Van der Rijt et al. [3] had not specifically addressed their research to the diagnosis of subclinical encephalopathy, subsequent studies [5], [6], [7], [8] showed that about 19–33% of cirrhotic patients without present overt hepatic encephalopathy (OHE) have EEG alterations according to Van der Rijt et al. criteria [3]. Moreover, the cirrhotic patients with such alterations were found to have an increased risk of both neuropsychological impairment [6], [7] and a reduced quality of life [9]. The existence of quantified-EEG alterations were found to have an ominous prognostic value on survival in a small study by Van der Rijt and Schalm [10]. However, a recent paper by Hartmann et al. [11] showed a poor prognostic value of subclinical hepatic encephalopathy defined as the presence of EEG or psychometric alteration in a series of cirrhotic out-patients with predominantly mild liver disease.
We, therefore, performed a study aimed at assessing the prevalence of EEG abnormalities in cirrhotic patients without OHE, and the clinical outcome of the patients with EEG abnormalities.
Section snippets
Patients
Cirrhotic patients without present OHE whose conditions were stable and who consecutively underwent quantified-EEG in our unit (a routine examination in our centre) were considered for the study. OHE was defined as encephalopathy clearly exceeding grade 1 according to Conn's criteria [12], and therefore requiring hospitalization. The patients recruited had normal orientation (personal identity, present situation, place and time) and were ambulant; however, patients with minor signs of
Results
The main demographic, clinical, biochemical and EEG data of the patients in the study group and the validation group are shown in Table 1. Three patients had had a spleno–renal shunt in both the study and validation groups, whereas no patient had undergone a transjugular intrahepatic portal systemic shunt or other portal–systemic shunt procedures either in the study or validation group.
Discussion
The EEG provides information on metabolic encephalopathies because it reflects neuronal electrogenesis which, in turn, is quite sensitive both to the influence of nutritive and energy-providing metabolic systems, and to the influence of electrolyte homeostasis and of the clearance of toxic substances [14]. However, information regarding the relationship between EEG and liver function in cirrhosis is scanty. Quero et al. [8] showed a trend towards a higher degree of EEG alterations in Child–Pugh
References (20)
- et al.
The electroencephalograph in liver disease
Lancet
(1957) - et al.
Objective measurement of hepatic encephalopathy by means of automated EEG analysis
Electroenceph clin Neurophysiol
(1984) - et al.
Spectral versus visual EEG analysis in mild hepatic encephalopathy
Clin Neurophysiol
(1999) - et al.
The diagnosis of subclinical hepatic encephalopathy in patients with cirrhosis using neuropsychological tests and automated electroencephalogram analysis
Hepatology
(1996) - et al.
Quantitative EEG analysis and survival in liver disease
Electroenceph clin Neurophysiol
(1985) - et al.
The prognostic significance of subclinical hepatic encephalopathy
Am J Gastroenterol
(2000) - et al.
Comparison of lactulose and neomycin in the treatment of chronic portal–systemic encephalopathy. A double blind controlled trial
Gastroenterology
(1977) - et al.
Chronic hyponatremia exacerbates ammonia-induced brain edema in rats after portacaval anastomosis
J Hepatol
(1998) - et al.
Elevation of intracranial pressure following transjugular intrahepatic portosystemic stent–shunt for variceal haemorrhage
J Hepatol
(1997) - et al.
Proton magnetic resonance spectroscopy studies on human brain myo-inositol in hypo-osmolarity and hepatic encephalopathy
Gastroenterology
(1994)
Cited by (209)
Current approaches to hepatic encephalopathy
2022, Annals of HepatologyEncephalopathy in Cirrhosis: Prevention and Management
2022, Journal of Clinical and Experimental HepatologyThe current pediatric perspective on type B and C hepatic encephalopathy
2022, Analytical BiochemistryGut-derived systemic inflammation as a driver of depression in chronic liver disease
2022, Journal of HepatologyClinical Implications, Evaluation, and Management of Hyponatremia in Cirrhosis
2022, Journal of Clinical and Experimental HepatologyHepatic encephalopathy and depression in chronic liver disease: is the common link systemic inflammation?
2022, Analytical Biochemistry