Brain electrical activity mapping of EEG for the diagnosis of (sub)clinical hepatic encephalopathy in chronic liver disease

Abstract

We studied the role of brain electrical activity mapping (BEAM) in the assessment of neuropsychiatric disturbances in 48 cirrhotic patients without clinical evidence of hepatic encephalopathy (no HE, n = 19), with subclinical HE (grade 0, denoting pathological psychometric tests, n = 13) and mild-to-moderate HE (grade I, n = 6; grade II, n = 10). Results were compared with 23 healthy controls. BEAM variables quantified were: (i) the peak frequency (PF); (ii) the amplitude of PF; and (iii) the topographic localization of the maximum peak amplitude digitized for quantification by using a coordinate system. Mean amplitudes and their topographic localization in the following frequency-bands were analysed: delta (1.0-3.5 Hz), theta (4.0-7.5 Hz), alpha 1 (8.0-9.5 Hz), alpha 2 (10.0-11.5 Hz), beta 1 (12.0-15.5 Hz), beta 2 (16.0-19.5 Hz), and beta 3 (20.0-23.5 Hz). The PF was significantly slower in all HE patients than in healthy controls (8.5 +/- 2.0 Hz v. 10.1 +/- 1.0 Hz, P< 0.001). Even in no HE, the PF was significantly slower than in controls (8.6 +/- 1.5 Hz v. 10.1 +/- 1.0 Hz, P< 0.01). No relevant topographic differences of PF were observed. The mean amplitudes of the following bands differed significantly between controls and patients: theta (increased in HE, P< 0.05), alpha 2 (decreased in HE, P< 0.05), and beta 2 and beta 3 (increased in HE, (P < 0.05). In HE patients, the topographic localization of all beta bands showed a significant shift from parieto-occipital areas to central areas of the cortex. We conclude that BEAM is a sensitive tool for detecting neuropsychiatric disturbances in cirrhotics with no HE and with subclinical HE. The combination of PF in the theta band, increased mean amplitude in the beta 2 band, and the localization of the latter band in the frontocentral area of the cortex is an objective and sensitive tool for identifying neuropsychiatric disturbances in 85% of cirrhotic patients with no HE. Further studies are required to determine the clinical implications of these abnormal findings in the absence of overt clinical symptoms.