Clinical neurophysiology of hepatic encephalopathy

Abstract

Background/objectives: Hepatic encephalopathy (HE) has relevant impact on the quality of life of patients and their caregivers and causes relevant costs because of hospitalizations and work days lost. Its quantification is important to perform adequate clinical trials on this relevant complication of cirrhosis and portal-systemic shunting. Clinical neurophysiology, which detects functional alterations of the nervous system, has been applied to the study of HE for over 60 years. This review aims at summarizing and clarifying the role of neurophysiologic techniques in the study of HE.

Methods: A narrative review was performed aiming at interpreting the cited papers and the techniques on the basis of their physiological and pathophysiological meaning.

Results: The potential role of EEG, quantified EEG, evoked potentials-both exogenous, endogenous and motor-have been clarified to the reader that may be unfamiliar with neurophysiology.

Conclusions: The EEG, reflecting the oscillatory changes of neural network is the preferable tool to detect and monitor HE, with the exception of its most severe stage, when EEG flattens. SSEP and MEP have indication to detect and monitor transmission alterations that are likely related to myelin changes and microedema.

Keywords: BAEPs, brainstem acoustic evoked potentials; EEG; EEG, electroencephalogram; EPs, evoked potentials; ERPs, event related potentials; HE, hepatic encephalopathy; MEG, magnetoencephalogram; MEPs, motor evoked potentials; SSEPs, somatosensory evoked potential; VEPs, visual evoked potentials; cirrhosis; evoked potentials; fVPS, flash visual evoked potentials; hepatic encephalopathy; neurophysiology; pVEPs, pattern reversal visual evoked potentials.

Figure 1

The EEG changes in HE. From the left to right (A): a normal EEG; B: low frequency, frontalized alpha activity with random theta waves; C: predominant theta activity with random delta waves; D: high voltage delta–theta activity with triphasic waves (inside circles), E: the EEG tends to flatten (the high voltage waves are gasping artefacts). Personal observations obtained by Micromed equipment.

Figure 2

Grade 3 HE in acute on chronic liver failure before MARS (on the left) and after MARS (on the right). On the left bursts of triphasic waves are detectable. On the right triphasic waves disappear in parallel with improvement of metal state (from 3 to 1). (Personal observation obtained by a Micromed EEG equipment—Mogliano Veneto, Italy).

Figure 3

A burst of intermittent rhythmic delta activity in a cirrhotic subject with a 7 Hz background frequency and clinical signs of grade one HE (Personal observation obtained by a Micromed equipment—Mogliano Veneto, Italy).

Figure 4

Potentials evocated by the auditory oddball paradigm in two age-matched subjects: a normal one (on the top) and a cirrhotic patient with minimal HE (on the bottom). The lines marked with flags represent the response elicited by the deviant (target and rare) stimuli, the other ones the responses elicited by the frequent stimuli. The peak of P300 in the normal subject is about 300 ms from the onset (three squares of 100 ms), in the patient with minimal HE the peak of P300 is about 480 ms. Personal observations obtained by a Micromed EEG equipment—Mogliano Veneto, Italy).